Pha 416 Exam 3 (Oncology)

Front 1

Generic of Avastin

Back 1

bevacizumab

Front 2

Generic of Erbitux

Back 2

Cetuximab

Front 3

Generic of Rituxan

Back 3

rituximab

Front 4

Generic of Gleevec

Back 4

Imatinib

Front 5

Generic of Herceptin

Back 5

trastuzumab

Front 6

Generic of Yervoy

Back 6

ipilimumab

Front 7

Generic of Tykerb

Back 7

iapatinib

Front 8

Pre treatment for monoclonal antibodies infusion:

Back 8

APAP, Benadryl, corticosteroid, and meperidine(regrugs and chills)

Front 9

MOA of Rituximab

Back 9

Binds to CD20+ antigen on B-lymphocytes
Antibody dependent cytotoxicity

Front 10

Consideration of Rituximab infusion:

Back 10

- First exposure is the worse
- it may take up to 8 hrs

Front 11

Toxicities of Rituximab

Back 11

Infusion related reactions
Possible anaphylactic reactions
(Pretreat APAP and diphenhydramine)
- Tumor lysis syndrome (black box warning)
Allopurinol and monitor electrolytes
- Reactivation of Hep B, CMV, etc…
(Must check for previous Hep B)

Front 12

MOA of Tositumomab

Back 12

Binds to CD20+ cells
Linked to Iodine-131

Front 13

Indication for Tositumomab

Back 13

NHL refractory to rituximab

Front 14

Toxicities of Tositumomab:

Back 14

Premedicate with APAP and Benadryl
Give thyro-protective agent: Potassium iodide (SSKI) drops at least one day prior to giving
Prolonged pancytopenia (nadir 4-7 WEEKS)
- Pregnancy category X
- High incidence of secondary malignancies

Front 15

MOA of ofatumumab

Back 15

Bind to CD20+ antigen on B-cells
Causes B-cell lysis

Front 16

Indication for ofatumumab

Back 16

CLL
Second line after rituximab

Front 17

Toxicities of ofatumumab

Back 17

Severe infusion reactions (44%) although is a human antibody.

Prolonged thrombocytopenia and neutropenia

Reactivation of Hepatitis B

Severe infections (70%) (even being a fully human AB)

Very long infusion administration ( 8-9 hrs)

Front 18

MOA of alemtuzumab

Back 18

Binds to CD 52+ on malignant lymphocytes

Front 19

Toxicities of alemtuzumab

Back 19

- PROLONGED immunosuppression

- HSV and PCP prophylaxis (fungal?)

- CMV reactivation (prophylaxis w/ ganciclovir)

Infusion related reactions

Front 20

Cell surface cycloprotein monoclonal antibodies:

Back 20

Rituximab
Ibritumomab tiuxetan
Tositumomab
Ofatumumab
Alemtuzumab

Front 21

Anti-angiogenesis agents (VEGF):

Back 21

Bevacizumab

Front 22

MOA of Bevacizumab:

Back 22

Binds to vascular endothelial cell growth factor in circulation

VEGF ligand binding antibody

Front 23

Toxicities of Bevacizumab

Back 23

May cause DVTs or PEs
GI perforation
Delayed wound healing
Thrombotic events
Hypertension
Bleeding
Proteinuria

Front 24

MOA of cetuximab

Back 24

Binds to cell surface of epidermal growth factor receptor (EGFR)

Prevents EGFR binding and signal transduction

Front 25

Indication for cetuximab

Back 25

Colon cancer (without KRAS mutation)
Head and neck

Front 26

EGFR should be avoided in the treatment of cancer with what specific mutation:

Back 26

K-RAS

Front 27

Toxicities of cetuximab

Back 27

Acneiform skin rash
N/V
Mucositis

Front 28

Characteristics of cetuximab rash:

Back 28

starts within 1st week
No bacteria found
Treatment:
- Creams
- Anti-inflammatory

Front 29

MOA of Panitumumab:

Back 29

Binds to EGFR similar to cetuximab
Used after cetuximab

Front 30

toxicities of panitumumab

Back 30

Acneiform skin rash
N/V
Mucositis

Front 31

Indication for panitumumab

Back 31

Colon cancer

Front 32

MOA of trastuzumab

Back 32

HER2/neu
Oncogene overexpressed in 25% breast Ca
Herceptin binds and leads to antibody dependent cellular cytotoxicity

Front 33

Indication for trastuzumab

Back 33

Breast Cancer that overexpress HER2/neu

Front 34

Toxicities of trastuzumab:

Back 34

DLT is cardiovascular
Not given in combination with Doxorubicin
Infusion reactions:
- Rash
- Myelosuppression

Front 35

MOA of pertuzumab

Back 35

HER dimerization inhibitor (HER2/neu receptor antagonist)

Front 36

Toxicities of pertuzumab:

Back 36

Left ventricular dysfunction (CHF) but it is still given in combination with trastuzumab

Rash
Myelosuppression
Pregnancy D: Fetal death and birth defects

Front 37

MOA of ipilimumab

Back 37

Increase T-cell activation and response

Front 38

Toxicity of ipilimumab:

Back 38

Severe and fatal immune reactions due to T-cell activation/proliferation
- Enterocolitis/diarrhea/abdominal pain
- High dose steroids for treatment

Front 39

How to recognized Tyrosine kinase inhibitors?

Back 39

AKA ...nibs = oral agents

Front 40

MOA of gefitinib and erlotinib

Back 40

Tyrosine kinase inhibitors
- Inhibit phosphorylation of EGFR (EGFR-TK)

Front 41

Indication for erlotinib

Back 41

NSCLC and pancreatic cancer (increase survival 12 days in combination with gemcitabine)

Front 42

Toxicities of erlotinib

Back 42

Diarrhea
Rash (acneiform)
Interstitial lung disease (SOB or pneumonia type symptoms), rare but fatal
CYP 3A4
- Increases INR

Front 43

Drugs that bind to CD20

Back 43

Rituximab
Ibritumomab tiuxetan
Tositumomab
Ofatumumab

Front 44

What VEGF stands for?

Back 44

Vascular endothelial growth factor

Front 45

MOA of imatinib:

Back 45

Inhibit bcr-abl tyrosine kinase
- Stops proliferation

Front 46

Toxicities of imatinib

Back 46

Myalgias/Arthralgias (affects compliance)
Myelosuppression
N/V
Edema (CHF)

Front 47

BCR-ABL tyrosine kinase inhibitors

Back 47

Imatinib
Dasatinib
Nilotinib
Bosutinib
Ponatinib

Front 48

Toxicities of Dasatinib and Nilotinib:

Back 48

- Toxicities and dosing similar to imatinib

- Don’t use with PPIS or H2

- QT prolongation black box warning

Front 49

Characteristic of Ponatinib

Back 49

BCR-ABL tyrosine kinase inhibitors
- 3rd generation
- Does target T3151 mutation (it can be used in CML resistant to the other TKIs

Front 50

MOA of Lapatinib

Back 50

Inhibits Her2/Neu phosphorylation

Front 51

Toxicity of Lapatinib

Back 51

Hand Foot syndrome

Front 52

MOA of Crizotinib

Back 52

ALK (anaplastic lymphoma kinase) tyrosine kinase

Front 53

Indication for Crizotinib

Back 53

ALK+ NSCLC
- EML4–ALK fusion
- Must have FDA approved test done to confirm ALK+

Front 54

Toxicity of Crizotinib

Back 54

Severe and fatal pneumonitis
Hepatotoxicity
QT-prolongation

Front 55

MOA of Vemurafenib

Back 55

Inhibits BRAF serine thireonine kinase

Front 56

Indication for Vemurafenib

Back 56

Malignant melanoma
- (V600E mutation of the BRAF gene)

Front 57

Drugs approved for renal cell

Back 57

Sunitinib
Sorafenib
Pazopanib
Axitinib
Temsirolius
Everolimus
Bevacizumab

Front 58

Toxicities of Sunitinib

Back 58

GI
Skin discoloration (yellowish)
CYP 3A4
Hypothyroidism (txt with levothyroxine)

Front 59

Toxicities of Pazopanib

Back 59

Severe and fatal hepatotoxicity—black box warning
Prolonged QT-intervals
Fatal hemorrhagic events
Hypertension
Hypothyroidism
GI perforations

Front 60

Agents that inhibit numerous TK including VEGF, platelet derived GF

Back 60

Sunitinib
Sorafenib

Front 61

MOA of Pazopanib and Axitinib

Back 61

Binds to VEGF, PDGFR, c-KIT, etc…

Front 62

Typical treatment for anticipatory N/V:

Back 62

Benzo
(Ativan) Lorazepam

Front 63

Type of N/V produced by cisplatin:

Back 63

Delayed N/V
The most emetic cancer medication

Front 64

High emetic drugs

Back 64

Cisplatin
Cyclophosphamide (> 1500mg/m2)
AC combination (doxorubicin/cyclophosphamide)
Dacarbazine/Nitrogen mustards

Front 65

Moderate emetic drugs

Back 65

Carboplatin
Most anthracyclines alone

Front 66

Low emetic drugs

Back 66

Taxanes
5-FU
Topoisomerase inhibitors

Front 67

5-HT3 antagonist agents used for N/V:

Back 67

Dolasetron
Granisetron
Ondansetron
Palonosetron

Front 68

Role of 5-HT3 antag. agents in the txt of N/V:

Back 68

Effective for prevention of ACUTE (first 24hrs) CINV

Prevention of post-op nausea and vomiting (PONV) and radiation induced N/V

Front 69

Palonosetron used:

Back 69

IV
prevention of acute and delayed in moderately emetogenic chemo

Front 70

Trade name for Dolasetron

Back 70

Anzemet

Front 71

Trade name for Granisetron

Back 71

Kytril

Front 72

Trade name for Ondansetron

Back 72

Zofran

Front 73

Trade name for Palonosetron

Back 73

Aloxi

Front 74

Preferred route of admin for 5-HT3 antag.

Back 74

Oral

Front 75

Dose of ondasetron

Back 75

Ondansetron 16 to 24 mg orally or 8 to 16 mg IV daily

Front 76

Dose of Dolasetron

Back 76

Dolasetron 100 mg PO QD

Front 77

Dose of Granisetron

Back 77

Granisetron 2 mg QD or 1mg BID

Front 78

Dose of Palonsetron

Back 78

Palonsetron 0.25mg IV x 1 dose

Front 79

Adverse effects of 5-HT antag.

Back 79

QT-prolongation
Constipation (pregnancy)
Diarrhea (chemo txt)

Front 80

Patient education on 5-HT3 antag.

Back 80

Take 30 minutes prior to chemo and on a scheduled basis after that OR 1x during surgery

PRN basis not recommended

Front 81

Used on corticosteroids in the txt of n/v

Back 81

Prevention of Chemotherapy induced N/V (not FDA-approved)

Synergistic with 5HT-3 and metoclopramide

Front 82

Doses of corticosteriods when adding to a 5HT-3 or alone:

Back 82

Highly emetogenic: 12-20 mg x 1 dose 30 min prior to chemo

Moderately emetogenic: 8-10 mg 1 dose 30 min prior to chemo

Continue 4-8 mg BID x ~3 days after chemo

Front 83

rare corticosteriod AE:

Back 83

Anal burning
(txt: slow infusion rate)

Front 84

Neurokinin-1 Receptor Antagonists agents:

Back 84

Aprepitant and Fosaprepitant (Emend)

Front 85

Uses of NK-1 antag.

Back 85

Used in combination with steroids and 5HT-3 for prevention of acute and delayed N/V associated with highly and moderately emetogenic chemotherapy (3 drug regimen for cisplatin)

Front 86

What kind of medications are affected by the use of NK-1 antag.?

Back 86

Oral contraceptives

Warfarin: it may derease INR

Front 87

Dose of Aprepitant

Back 87

125mg PO day 1

80mg PO day 2

80mg PO day 3

Front 88

Dose of Fosaprepitant

Back 88

150mg IV once

Front 89

Dose of dexamethasone for high emetic chemotherapy:

Back 89

12mg IV day 1

8mg IV/PO day 2

8mg IV/PO on days 3 and 4 (if fosaprepitant is used then BID)

Front 90

When does aprepitant should be given to patients?

Back 90

1 hour prior to chemo with the 5-HT3 antag. and the corticosteriod

Front 91

Aprepitant AE:

Back 91

Diarrhea / constipation

Hiccups (may use a dopamine antagonist for txt)

Bradycardia

Front 92

Most commonly used dopamine antagonists:

Back 92

Prochlorperazine (Compazine)

Promethazine (Phenergan)

Metoclopramide (Reglan)

Front 93

Dose of Prochlorperazine

Back 93

10mg IV/PO Q6H scheduled or PRN
IV/PO/PR

Front 94

Dose of Promethazine

Back 94

12.5-25 mg Q4-6 H scheduled or PRN
Iv/PO/PR

Front 95

Dose of Haloperidol

Back 95

Haldol: 1-3mg IV/PO q 2-4 H prn

Front 96

Dose of metoclopramide

Back 96

10-40mg IV/PO Q6H With higher doses consider diphenhydramine 25-50mg to prevent EPS

Front 97

SE of metoclopramide

Back 97

EPS and excessive sedation

Irreversible tardive dyskinesias

Front 98

SE of droperidol

Back 98

black box warning for QT prolongation

Front 99

SE of promethazine

Back 99

Severe extravasation can occur

Must dilute with 10 ml NS if giving IV

Try to use oral if possible

Front 100

Dose of lorazepam

Back 100

Lorazepam 1-2mg IV/PO/SL q4-6 H prn OR 1 dose prior to chemo

Front 101

Prevention of CINV with highly emetogenic drugs:

Back 101

Aprepitant + 5-HT3 antagonist + dexamethasone

Front 102

Prevention of CINV with moderately emetogenic drugs:

Back 102

5-HT3 antagonist + dexamethasone +/- aprepitant

Front 103

Prevention of CINV with low emetogenic drugs:

Back 103

Dexamethasone or prochlorperazine or metoclopramide

Front 104

Prevention of CINV with minimal emetogenic drugs:

Back 104

None

Front 105

Options for breakthrough N/V:

Back 105

Dopaminergic agents

Haloperidol

Dronabinol

(Scheduled medications)

Front 106

How 5-HT3 antag. should be used in multiple day chemo regimens?

Back 106

Every day chemo is given a 5-HT3 antagonist should be given

(for moderate to highly emetic drugs)

Front 107

Agents used on pregnancy induced N/V

Back 107

Histamine antagonists and Phenothiazines are effective and equal to 5HT-3 in efficacy

Front 108

What is the name of the cells used to identify HL?

Back 108

Reed-Sternberg cells
(Multi-nucleated giant cells)

Front 109

Signs and Symptoms of HL:

Back 109

Painless adenopathy usually in lymph nodes above the diaphragm (cervical)
Orderly spread from one node to contiguous node

Front 110

What are B-symptoms?

Back 110

Fever
Unexplained weight loss
Night sweats

Front 111

Stage I HL:

Back 111

Single node or site

Front 112

Stage II HL:

Back 112

Two or more lymph node or sites on same side of diaphragm

Front 113

Stage III HL:

Back 113

Lymph node involvement on both sides of diaphragm

Front 114

Stage IV HL:

Back 114

Diffuse or disseminated involvement of organs/tissues

Front 115

What is the meaning of A, B, and X in HL?

Back 115

A = No fever (asymptomatic)

B = B-symptoms

X = Bulky disease (nodal mass >10 cm)

Front 116

Prognosis factors in HL:

Back 116

Serum albumin (< 4 g/dL)
Hemoglobin (< 10.5 g/dL)
Male
Stage IV disease
Age (> 45 yo)
Leukocytosis (WBC >15,000/mm3)
Lymphocytopenia (< 600/mm3)

Front 117

ABVD regimen:

Back 117

Doxorubicin (Adriamycin) 
Bleomycin (pulmonary toxicity)
Vinblastine (myelosuppression)
Dacarbazine (N/V)

Front 118

Treatment of relapsing HL:

Back 118

ABVD if relapse is more than 12 months later

Brentuximab (CD30+ antibody-conjugate used if two chemo regimens failed or failed stem cell transplant)

Front 119

Short term Effects of treatment for HL:

Back 119

Infection
Tumor Lysis Syndrome (hydration and electrolytes)
Pulmonary function
Cardiac function
Mycositis
Neurotoxicities

Front 120

Overall survival of HD:

Back 120

Good prognosis:
Stage I: 90-95%
Stage II: 90-95%
Stage III: 80-85%
Stage IV: 60-70%

Front 121

Incidence for NHL:

Back 121

Age: average 66yo
Males > females
Whites > blacks

Front 122

Risk factors for NHL:

Back 122

H. pylori, HIV, EBV, HHV-8
Chemicals exposures
Immune dysregulation
Chromosomal abnormalities

Front 123

What are the most common types of NHL:

Back 123

Diffuse Large B cell Lymphoma

Follicular lymphoma

Front 124

What type of lymphoma is caused by H. pylori?

Back 124

MALT lymphoma
(Mucos Assoc Lymphoid Tissue )

Front 125

Type of indolent lymphoma:

Back 125

Follicular
(hard to cure)

Front 126

Type of Highly aggressive lymphoma:

Back 126

Burkitt's lymphoma
(curable but tumor may double in size in 48 hrs)

Front 127

What type of regimen can be used for a indolent lymphoma advance disease (stage III and IV):

Back 127

No standard therapy

Rituximab based therapy

Front 128

Regimen for DLBC lymphoma:

Back 128

R-CHOP

Front 129

What does R-CHOP stands for?

Back 129

Rituximab - (reactivation of HepB)
Cyclophosphamide (renal function)
doxorubicin (hydroxydanorubicin) (liver function)
vincristine (neuropathies)
prednisone (blood sugar)

Front 130

additional therapy when using R-CHOP:

Back 130

Rituximab as maintenance
CNS prophylaxis with methotrexate

Front 131

Length of therapy using R-CHOP

Back 131

6 cycles

Front 132

Characteristics of Tumor Lysis syndrome:

Back 132

High potassium
High phosphate
High uric acid
Low calcium

Front 133

Treatment of high uric acid:

Back 133

Allopurinol:
- affects only new production
- takes days to have effect

Rasburicase:
- affects new and existent production
- Takes just hours to work

Front 134

Difference in treatment between Acute and chronic leukemias:

Back 134

Acute are a medical emergency while chronic may or may not require immediate treatment.

Front 135

What type of leukemia is most common in childhood?

Back 135

ALL

Front 136

Prognostic risk factors for ALL:

Back 136

Age (less than 1 and more than 10= high risk)

WBC (more than 50K = high risk)

Philadelphia chromosome (high risk)

Male

Front 137

Treatment of ALL:

Back 137

Remmision induction (4 weeks)

Consolidation (4weeks)

Delayed intensificacion (3-9 mo)

Maintenance (2-3 yrs)

CNS prophylaxis given in all phases

Front 138

REmission induction in ALL txt:

Back 138

Vincristine IV
Dexamethasone PO
L-asparaginase (pegaspargase)

If High risk add to standard:
Daunorubicin or doxorubicin IV

Front 139

What are the drugs for CNS prophylaxis in ALL:

Back 139

Intrathecal cytarabine, hydrocortisone and/or methotrexate

Front 140

What phase of treatment is important in ALL but it is not used in AML?

Back 140

Maintenance phase (2-3 yrs)

Front 141

Drugs used in maintenance therapy for ALL:

Back 141

Mercaptopurine po q evening
Methotrexate po or IM q week
Dexamethasone 5 days/month
Vincristine IV q month
Intrathecal meds q 3 months

Front 142

What is the AML that has a better prognosis?

Back 142

M3 acute promyelocytic leukemia

Front 143

Treatment phases for AML:

Back 143

Remission induction

Consolidation (2-4)

(No maintenance phase)

Front 144

Standard induction of AML:

Back 144

7 + 3
7 days of continuous infusion cytarabine (low dose)

3 days of Idarubicin or Daunorubicin

SE: prolonged neutropenia

Front 145

Consolidation treatment for AML:

Back 145

High dose cytarabine

SE: Conjuctivitis (steroid eye drops) and Cerebral toxicity (test before every dose)

3-4 cycles

Front 146

AML M3 treatment:

Back 146

All-trans retinoic acid (ATRA) (PO)
- differentiation syndrome

Arsenic trioxide (IV)
- QT prolongation
- Differentiation syndrome

Front 147

Role of SCT in leukemia treatment:

Back 147

For relapse disease especially for ALL in young patients

Front 148

What causes CML:

Back 148

Philadelphia Chromosome Abnormality

Front 149

What is the translocation related to philadelphia chromosome:

Back 149

BCR-ABL that encodes for a tyrosine kinase that has 100x more actiivty than the normal.

Front 150

Effects of BCR-ABL translocation:

Back 150

Increases proliferation
Affects differentiation
Blocks apoptosis

Front 151

What Hematologic response indicates?

Back 151

Normalization of peripheral blood count
WBC < 10 x 10^9/L
Platelets <450 X 10^9/L
No immature cells

Front 152

What Cytogenetic response inidicates?

Back 152

Complete: elimination of Ph+ cells

Front 153

What Molecular response indicates?

Back 153

Absence of bcr-abl by RT-PCR

Front 154

What is hydroxyurea used for in CML?

Back 154

Used to reduce high circulating WBC and all cell lines
(for short term therapy)

Front 155

First line therapy drugs for CML

Back 155

Imatinib mesylate (STI 571; Gleevec)
Dasatinib (Sprycel)
Nilotinib (Tasigna)

Front 156

Dosage of gleevec:

Back 156

400mg/day with food and water
CHR: 3 mo
CCR: 9-12 mo
Few achieve molecular remission

Front 157

SE for Gleevec:

Back 157

Myelosuppression
Rash
GI side effects
Edema
Arthralgias and myalgias
Headaches
Rare cardiotoxicity/CHF

Front 158

What TKI are used in patient that developed mutations or resistance to gleevec?

Back 158

Dasatinib and Nilotinib
2nd generation tyrosine-kinase inhibitors
Indicated first-line for chronic phase, accelerated and blast crisis

Front 159

SE of dasatinib:

Back 159

Pleura effusions and bleeding

Avoid PPI and H2 blockers

Front 160

SE of nilotinib:

Back 160

QT prolongation

take on empty stomach

Front 161

Bosutinib indication:

Back 161

2nd generation bcr-abl TKI
Indications: CML that failed 1 TKI

Front 162

Ponatinib indication:

Back 162

BCR-ABL tyrosine kinase inhibitors
3rd generation
Does target T3151 mutation

Indications: CML that failed 1 TKI

Front 163

What is the only option for cure for CML?

Back 163

Allogeneic stem cell transplant

Front 164

Characteristics of CLL:

Back 164

Indolent disease

Elderly patients

Many times patient forgo treatment

Front 165

When to treat CLL:

Back 165

Treatment would be very aggressive if it is diagnosed in younger patients and/or it presents molecular markers

Front 166

What drug to use in the treatment of CLL if patient has deletion of p17?

Back 166

alemtuzumab

Front 167

If a CLL patient is younger than 70 what is the treatment:

Back 167

FCR:
- Fludarabine
- cyclophosphamide
- rituximab

Front 168

Risk factors for colon cancer:

Back 168

Age
Family hx
Personal hx of breast, ovarian, or endometrial cancer
Colon polyps
IBD (especially Ulcerative colitis)
Genetic predisposition

Front 169

Prevention of colon cancer:

Back 169

High-fiber; low-fat diet
Chemoprevention:
- Calcium
- Folate
- COX-2
- NSAIDS

Front 170

Screening for Colon Cancer

Back 170

Start at 50 yo
- FOBT = once a year
- Digital rectal exam = once a year
- Flexible sigmoidoscopy = q 5 yeats
- Colonoscopy = q10yrs

Front 171

Common S/S of advance colon cancer:

Back 171

Change in bowel habits
Rectal bleeding
Abdominal pain
Weight loss

Front 172

How many node are biopsied in the diagnosis of colon cancer?

Back 172

All 12 nodes

Front 173

What mutation has to be tested for in colon cancer?

Back 173

K-RAS (Unresponsive to EGFR-inhibitors: Cetuximab or panitumumab)

Front 174

Stage I colon cancer txt:

Back 174

Superficial lession

Surgery and nothing else

Front 175

Stage II colon cancer txt:

Back 175

Surgery and nothing else

Front 176

Stage III colon cancer txt:

Back 176

Lymph node involvement

Surgery AND chemo right after

FOLFOX or CapeOX

Front 177

What adjuvant therapy mean:

Back 177

Therapy given after surgery with the intention to cure the patient. No place in metastatic disease.

Front 178

What does FOLFOX stands for?

Back 178

Oxaliplatin IV over 2 hours on Day 1 (PN - cold)
Leucovorin IV over 2 hours on Days 1 and 2
5-FU IV bolus and continuous infusion (48 hours)
Repeat every two weeks

Front 179

what does CapeOX stands for?

Back 179

Capacitabine (PO) (hand foot symdrome)
Oxaliplatin (PN)

Front 180

What drugs should not be used for adjuvant colon cancer therapy?

Back 180

irinotecan
cetuximab
bevacizumab

Front 181

Why is Bevacizumab never given right after surgery? One more time - what's the trade name?

Back 181

Bevacizumab delays wound healing (give 6 weeks later). Avastin is the Trade name.

Front 182

Stage IV colon cancer txt:

Back 182

incurable (Unless resectable liver mets)

Chemotherapy is mainstay:
FOLFOX
FOLFIRI
CapeOX
Infusional 5FU/LV
FOLFOXIRI

always add biologics bevacizumab, cetuximab or panitumumab

Front 183

Treat of isolated hepatic mets in colon cancer:

Back 183

Single lesions resected
Hepatic artery infusion of 5-FU or FUDR
Chemoembolization (mixed in Gelfoam)
Mitomycin C
Doxorubicin
Cisplatin

Front 184

Important signs for skin cancer:

Back 184

A sore that does not heal

Obvious change in wart or mole

Front 185

ABCDE of melanoma:

Back 185

A: Asymmetric
B: Irregular Borders
C: Color of lesion (not uniform)
D: Diameter > 6mm or size of pencil eraser
E: Evolving characteristics of lesion

Front 186

Guidelines for surgery in melanoma patients:

Back 186

<1 mm in thickness, require 1 cm margin
2 mm in thickness, require 2 cm margin

Front 187

Role of chemotherapy in melanoma:

Back 187

Not recommended

Front 188

Treatment options for metastatic melanoma:

Back 188

Clinical trial
Ipilimumab
Vemurafenib (BRAF mutation)
Aldesleukin (IL-2)

chemo is 2nd or 3rd option

Front 189

MOA of ipilimumab

Back 189

Increase T-cell activation and response to stimulate immune reaction

Front 190

SE of ipilimumab

Back 190

Severe enterocholitis (txt high dose steroids)

Immune AE

Front 191

What is the common mutation in melanoma:

Back 191

BRAF (involve in cell growth) 45%

Front 192

MOA of Vemurafenib

Back 192

Inhibits BRAF serine threonine kinase

- mutation has to be confirmed by an FDA approved test

Front 193

How many doses of IL-2 are recommended for the txt of metastatic melanoma?

Back 193

14 doses
(but most patients cannot tolerate more than 10-12)

Front 194

Survival rates with melanoma:

Back 194

Localized dz: 98% (5yr)
Regional spread: 60%
Metastatic spread: 16%

Front 195

How to calculate SPF:

Back 195

# of min normally burn x (spf) = min of protection from the sun

Front 196

How much UVB is blocked by SPF 15?

Back 196

93%

Front 197

How much UVB is blocked by SPF 30?

Back 197

97%

Front 198

Indication for Vismodegib:

Back 198

Basal cell carcinoma; after failing other options

Front 199

What is the type of skin cancer that is serious and fatal?

Back 199

Melanoma
(non-melanoma rarely mets)

Front 200

Define pharmacogenomics:

Back 200

differences in MULTIPLE genes influence variability in drug response (i.e., efficacy and toxicity)

Front 201

CYP 2D6:

Back 201

-Metabolizes 25-50% of drugs

- Substrates:
Antidepressants
Antiarrhythmics
B-adrenergic antagonists
Prodrugs such as codeine, tramadol and tamoxifen

Front 202

CYP 2C19:

Back 202

Poor metabolizers common in Chinese and Japanese

Drugs involved include:
Omeprazole
Voriconazole
Phenytoin
Clopidogrel

Front 203

CYP 2C9:

Back 203

2-10% are homozygous for low-activity

Drugs metabolized:
- Warfarin
- Losartan

Front 204

VLOR and Warfarin pharmacogenomic relationship:

Back 204

Polymorphisms of VKOR account for 25-30% of dose variability
Some patients may require >100mg/week or never achieve anticoagulation

Front 205

What two drugs can be used for medullary thyroid cancer?

Back 205

Vandetinib and Cabozantinib.